#27 Season 1 Listener Mailbag
Join Cyrus and Nick as they review listener questions and feedback from season one of Critical Care Time! Where did we goof up? Where did we hit the "Mark"? Give this episode a listen as we investigate a potpourri of clinically relevant topics courtesy of YOU - our incredible audience whom we are so thankful for.
Show Notes:
Limitations of non-invasive cardiac monitoring
Justin Writes “Just wanted to make a comment towards your praise of non-invasive cardiac monitoring.
These devices seem to be gaining a lot of popularity, starting in anesthesia and now in many ICUs.I would give a strong warning of caution, however; by and far they have NOT been validated in the critically ill, the majority of studies are funded by the companies, the accuracy of many of the numbers given (like CO) are extrapolated and have been shown to NOT be accurate when compared to animals with invasive monitors in place and many of the studies have parameters (like TV of at least 8cc/kg) that make its use NOT applicable to most ICU patients anyway.“Three points about non-invasive cardiac output monitoring:
1. Just because a test tells you that a person is volume responsive does not mean that you should give them volume! The decision to give volume depends on multiple factors:
is it safe to give volume? (is this person fluid tolerant?)
Is this person hypoperfusing and would increasing their cardiac output be beneficial?
Is volume the best intervention? Someone with a GI bleed may be “fluid responsive” but the treatment is blood products not fluid.
2. Using a test of volume responsiveness is probably better than using no test at all but… each of these tests have limitations. You have to pick a test - or better yet tests - that is applicable to your patient.
It’s important to interpret the results of these tests in the context of your patient.
It’s important to integrate all the data together and put the volume responsiveness in the context of other tests.
3. I think some of these tests are great and are truly useful clinically, but I agree they have limitations.
Many tests are only applicable only in narrow circumstances (e.g. tidal volume 8 ml/kg, sinus rhythms, intubated with no spontaneous respirations).
The quality of the evidence is variable. Lots of small studies. We need better studies of fluid responsiveness in general, and a network meta-analysis would be very helpful.
Bottom line:
All tests have limitations, particularly tests of complex physiology like volume responsiveness. In general, dynamic tests of volume responsiveness are better than static ones, and invasive tests are better than non-invasive ones.
Multiple tests are better than just one.
And most importantly, “just because a test tells you that someone is volume responsive doesn’t mean you need to or ought to give volume” Just because you have a fancy gizmo doesn’t mean you don’t have to think! In fact the more fancy gizmos you have the more you need to think!
See this ICU OnePager for more about Fluid Responsiveness & Fluid Tolerance
Albumin, Gut Edema, & Loop Diuretics
Several listeners wrote to us about this question.
Does hypoalbuminemia really effect loop diuretic delivery?
There is a human double blind cross over study from 1976 showing improved diuresis with bumetanide over furosemide in people with nephrotic syndrome. On the other hand, several more modern studies have found little correlation between serum album and effectiveness of furosemide.
A study in analbuminemic rats found that bumetanide had 3x the binding to alpha and beta globulins as furosemide. Bumetanide produced more diuresis than furosemide in these hypoalbuminemic rats.
Important caveat that rats lacking all albumin are not necessarily interchangable with low albumin due to illness in humans.
The oral absorption of furosemide is extremely variable.
Furosemide is absorped in the stomach and duodenum. Changes in gastric pH, gastric contents, perturbations in mucosal blood flow, and changes in GI motility can all affect absorption of PO furosemide.
Other loop diuretics - torsemide and bumetanide - appear to have less variable gastric absorption.
Systemic Vascular Resistance, Compliance, and Pulse Pressure
Two listeners point out an oversimplifcation we made in the episode of about shock.
They point out that because of the relationship between pulse pressure (PP) and compliance (CC) you might expect a low PP in sepsis due to the increased compliance of the blood vessels.
“PP = SBP - DBP
PP ∝ Stroke Volume / Compliance”
There are a few areas where we oversimplified our explanation:
The cardiovascular system is dynamic and changes in afterload affect cardiac output.
Therefore when the afterload decreases the stroke volume increases. This is because there is less pressure in the aorta to pump against so the LV is able to eject more blood.
The problem is that ventricular-arterial coupling is complex and non-linear!
A small increase in compliance can lead to a larger increase in stroke volume, thus pulse pressure can increase.
The pattern of pulse pressure increase is also informative:
In people with stiff arteries due to arterioscelerosis, you typically see elevated diastolic and systolic pressures, but with a greater increase in systolic than diastolic.
During exercise, systolic blood pressure increases but diastolic doesn't. This also causes increased pulse pressure.
In sepsis or liver failure, where the issue is vasodilation, the diastolic blood pressure drops dramatically. This also causes an increased pulse pressure.
When you see widened pulse pressure with low diastolic it suggests vasodilation is contributing. (not necessarily true of the other patterns)
Where/how you measure blood pressure also matters.
The vascular tone in your aorta and big arteries tends to be determined by elastin fibers (unaffected by vasodilation), whereas the tone in your smaller arteries and arterioles is determined by smooth muscle contraction (altered in vasodilation).
Therefore, vasodilation tends to have more of an effect peripherally rather than centrally.
Experiments in pigs confirm that pulse pressure widens in early sepsis, put only in peripherally measured BP. (MAP was similar in radial, femoral, and aortic sites)
Femoral versus radial arterial lines
Nick & Cyrus got involved in a twitter debate about “when to swap a [working] radial arterial line for a femoral line". The argument was that radial lines become “inaccurate” in shock. We strongly disagree with this argument & the practice of routinely performing additional invasive procedures.
Several reasons
In most people the difference between radial and femoral measurements of MAP is small.
A meta-analysis of ~1600 patients found the mean difference in MAP between femoral and radial arterial lines was 3.5 mmHg.
Even studies that examine specifically patients in refractory shock, only reported a difference mean difference of 7.6 mmHg.
If you understand that the radial arterial line may read slightly lower, you can interpret that MAP reading in context.
For example, if someone has a MAP of 55 mmHg radially but is making urine, clearing lactate, and mentating, this is probably equivalent to a MAP of 60 mmHg femorally.
The risks of femoral cannulation are low but non-trivial.
Femoral access limits mobility in ICU patients and may have higher infection risk.
There are also some procedural risks including retroperitoneal hemorrhage.
Performing an unnecessary procedure has only downside.
Vasopressor Nomenclature
GT points out the we should avoid the 1:x,000 nomenclature when describing epinephrine. This is needlessly confusing and potentially dangerous. Instead use standard concentration nomenclature. For example:
Low dose pushes of epinephrine, used in CALS-S codes, is typically 10 mcg/ml.
Standard dose pushes, used in ACLS codes, are 1 mg in 10 ml (or 100 mcg/ml)
SQ epinephrine, used in anaphylaxis, is 1 mg/ml (or 1000 mcg/ml).
M Birch writes “Great talk but please don’t conflate adrenergic and catecholamine. A catecholamine must have a catechol ring. Phenylephrine doesn’t and is not a catecholamine.”“
This is absolutely correct. We stand corrected. Thanks!
Simple vs tension pneumothorax
Stormblest had a questions about why only some pneumothoraces become tension. Several factors are involved:
1. Size of the Pneumothorax. A small collection of air in the pleural space may not significantly impair lung function or cardiovascular status. The lung may still be able to expand adequately, and there might be no significant shift of mediastinal structures. Larger pneumothoraces have a higher potential to compromise lung function, but whether they lead to tension physiology depends on other factors like the rate of air accumulation and the presence of a one-way valve effect.
2. Rate of Air Accumulation If air enters the pleural space slowly, the body might be able to compensate. The pleural pressure may not rise rapidly enough to cause a shift in mediastinal structures or significant cardiovascular compromise. A rapid influx of air is more likely to create high intrapleural pressure quickly, leading to tension physiology with associated hemodynamic instability.
3. Presence of a One-Way Valve Mechanism Tension pneumothorax typically occurs when there is a flap-like tear in the pleura that acts as a one-way valve, allowing air to enter the pleural space but not escape. This results in progressive accumulation of air and increasing pressure. In the absence of a one-way valve mechanism, air may still be able to exit the pleural space or the pressure may not build up to critical levels.
4. Communication with the Atmosphere (Open vs closed Pneumothorax). If there is a direct communication with the atmosphere (e.g., through an open chest wound), air can move freely in and out of the pleural space, preventing the development of high pressure. A closed pneumothorax without a significant one-way valve effect might not lead to tension physiology.
5. Compensatory Mechanisms. The body can sometimes compensate for a certain degree of intrapleural pressure. This compensation can prevent the shift of mediastinal structures and the compression of major vessels, thus averting tension physiology.
6. **Underlying Lung and Cardiovascular Health: Patients with healthy lungs and cardiovascular systems may better tolerate a pneumothorax without developing tension physiology compared to those with preexisting conditions.
Remember that tension is a physiological consequence of air accumulation. This is why its a clinical (not radiographic) diagnosis!
Why STANDARD GEOMETRY VL is better even in contaminated airways
Sntheticguitar writes “To Nick’s point about how he can’t think of a situation where DL is superior, my opinion is DL is better in bleeding airways or copious secretions. That camera is pretty small on the VL devices and a drop of blood/spit can really gum up your view.”
We agree that DL might be better if you we using hyperagulated VL and you lost your view because the camera was blocked. We generally do not recommend hyperangulated VL in patients with secretions or bleeding for exactly this reason.
On the other hand, if you use standard geometry VL you even if the image is obscured its still usable as DL. You haven’t lost anything, and potentially you’ve gained a lot. (improved view, higher probability of first pass success, etc)
To put this another way: the Degraded performance of standard geometry VL is the same at DL.
To recycle the joke NICK stole from Mitch Hedberg “A escalator can never brake, it’s just stairs”
“Standard geometry VL can’t brake, it’s just DL.”
Bag valve vs ventilator during cardiac arrest
Regarding our episode on Running a code: Jamshaid Khan writes “If the patient is already on vent before going into arrest, do you recommend taking the patient off vent and on ambu bag during CPR or. Just continue ventilating on previous settings and turning fio2 to 100%.”
There are pros/cons to each method. A BVM is simpler and requires less skill to setup/use. A ventilator is more likely to deliver appropriate volumes and pressures and does not require breaking the circuit.
In general simplicity is preferable, though there are circumstances (avoiding loss of recruitment, limited staffing present) where remaining on the ventilator may be advantageous.
Audio
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Teran F, Prats MI, Nelson BP, et al. Focused transesophageal echocardiography during cardiac arrest resuscitation: jacc review topic of the week. J Am Coll Cardiol. 2020;76(6):745-754.
Arntfield R, Lau V, Landry Y, Priestap F, Ball I. Impact of critical care transesophageal echocardiography in medical-surgical icu patients: characteristics and results from 274 consecutive examinations. J Intensive Care Med. 2020;35(9):896-902.
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Undifferentiated Shock
Cardiac Arrest